PULMONARY ARTERY CONSTRICTION IN THE CAT: 
A MODEL FOR VENTRICULAR HYPERTROPHY 
AND CONGESTIVE HEART FAILURE 
J. F. Spann, Jr.* and G. M. Lemole" 
The cat offers an excellent model to study hypertro- 
phy and congestive heart failure. By banding the pul- 
monary artery and allowing hypertrophy and/or 
congestive heart failure to occur, it is possible to accu- 
rately measure and record the changes in contractility 
by measuring the force velocity, relationship, Vmax and 
length-tension curves. Because of the unique anatomy 
of the papillary muscle of the right ventricle of the cat, 
accurate in vitro measurements can be made in the pap- 
illary muscle bath. These can be compared to in vivo 
intact ventricle preparations and the hemodynamical al- 
terations studied and analyzed in light of the in vitro 
measurements. This method also allows us to obtain 
the tissue for biochemical analysis in order to measure 
substrate availability, energy storage, energy utilization 
and conversion, and excitation-contraction coupling. 
Lastly, we can record the "effects of inotropic inter- 
vention by use of paired electrical stimulation, changes 
in frequency of contraction and the addition of stro- 
phanthidin and norepinephrine in the normal, hypertro- 
phied and failing heart." 
INTRODUCTION 
Ventricular hypertrophy and congestive 
heart failure have deen induced in dogs,^ 
guinea pigs^ and rabbits^ and such experimen- 
tal models have provided considerable insight 
into these pathologic states. However, a quanti- 
tative description of the contractile state of the 
cardiac muscle isolated from the hypertrophied 
or failing heart has not been available. The cat 
offers unique advantages for analyzing the con- 
tractile state of the myocardium in hypertrophy 
with and without congestive heart failure. This 
animal is suitable for hemodynamic studies, 
measurement of the contractile performance of 
the intact ventricle,'* and the papillary muscle 
from the right ventricle is small enough to per- 
mit in vitro oxygenation and its fibers are ori- 
ented in parallel and thus, allow quantitative 
* Chief, Section of Cardiology, Program Manager, Cardiopulmon- 
ary Program, Professor of Medicine, Temple University Health 
Sciences center. 
** Chief, Section of Cardiac and Thoracic Surgery, Associate 
Professor of Surgery, Temple University Health Sciences Center. 
definition of the heart muscle function per unit 
of muscle mass. Further, the functional charac- 
teristics of the cat papillary muscle preparation 
have been described in detaiP and have suffi- 
cient uniformity to allow a meaningful compar- 
ison of the myocardial contractile state of one 
group of cats to that of another group. To pro- 
vide the animal model for such studies, a 
method of production of right ventricular hy- 
pertrophy with and without congestive heart 
failure in the cat was developed. This technique 
imposes a chronic pressure load on the right 
ventricle by reduction of the lumen of the su- 
pravalvular portion of the main pulmonary ar- 
tery with a constricting clip. 
BACKGROUND 
The pathophysiology which attends both car- 
diac hypertrophy and congestive heart failure 
has been a subject of intense interest and inves- 
tigation for many years. Considerable attention 
has been focused on the clinical manifestations 
of heart failure, the hemodynamic alterations of 
the failing heart as a pump, and the deleterious 
effects of heart failure on other organ systems 
such as the kidney. More recent investigations 
have emphasized an understanding of the hy- 
pertrophied and failing heart as abnormal car- 
diac muscle with secondary emphasis on the 
function of the heart as a pump." It has now be- 
come quite apparent that considerable depres- 
sion of intrinsic myocardial function may be 
present with no apparent alteration in hemo- 
dynamic function: elevation of ventricular 
end-diastolic pressure, increased arteriovenous 
oxygen differences, and decreased cardiac out- 
put are frequently late manifestations of failing 
myocardial function or, indeed, can be due to 
extra myocardial factors. For example, an in- 
crease in end-diastolic pressure is not a reliable 
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